| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
| Targets |
PI3K
Glaucocalyxin A targets the PI3K/Akt signaling pathway, a key regulator of cell survival, proliferation, and apoptosis. By inhibiting PI3K/Akt phosphorylation, the compound suppresses GLI1 nuclear translocation and activation, leading to apoptosis induction. It also activates the mitochondrial apoptotic pathway by increasing the Bax/Bcl-2 ratio, triggering intracellular ROS generation, reducing mitochondrial membrane potential (MMP), and inducing caspase-9 and caspase-3 cleavage. The compound inhibits platelet p-selectin secretion and integrin activation via the GPVI pathway. |
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| ln Vitro |
Glaucocalyxin A causes apoptosis by activating the mitochondrial apoptotic pathway through a number of processes, including elevating the Bax/Bcl-2 ratio, inducing the production of intracellular reactive oxygen species (ROS), decreasing mitochondrial membrane potential (MMP), and causing caspase-9 and caspase-3 cleavage[1].
In vitro, Glaucocalyxin A induces apoptosis in human bladder cancer cells, osteosarcoma cells (HOS and MG-63), non-small cell lung carcinoma cells, and triple-negative breast cancer cells (MDA-MB-231). It inhibits Akt phosphorylation, suppresses proliferation, and promotes apoptosis in a dose-dependent manner in cancer cells but not in normal glial cells. In osteosarcoma cells, the compound inhibits GLI1 activation via PI3K/Akt pathway regulation. It also inhibits collagen-stimulated tyrosine phosphorylation of Syk, LAT, and phospholipase Cγ2 in the GPVI pathway. |
| ln Vivo |
Specific in vivo data for Glaucocalyxin A are limited in the available literature, but the compound shows promising antitumor activity in preclinical models. Given its potent in vitro anticancer effects and ability to induce apoptosis through multiple pathways, the compound is expected to demonstrate efficacy in xenograft models of various cancers. Its antiplatelet and antithrombotic activities suggest potential for in vivo studies in thrombosis models. The compound's anti-inflammatory activity could be evaluated in models of inflammation. However, specific published in vivo protocols are not detailed.
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| Enzyme Assay |
The PI3K/Akt pathway modulation is assessed by Western blot analysis. Cancer cells (e.g., HOS, MG-63, MDA-MB-231) are treated with Glaucocalyxin A at various concentrations for 24-48 hours. Cell lysates are prepared and analyzed for PI3K, p-Akt (Ser473), total Akt, and downstream targets by Western blot using specific antibodies. Apoptosis is assessed by measuring caspase-3/9 activity, Annexin V/PI staining, and DNA fragmentation. ROS production is measured using DCFH-DA, and mitochondrial membrane potential is assessed using JC-1 dye.
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| Cell Assay |
For cellular studies, cancer cell lines such as HOS, MG-63 (osteosarcoma), MDA-MB-231 (breast cancer), and NSCLC cell lines are cultured in appropriate media supplemented with 10% FBS at 37°C in 5% CO₂. Cells are treated with Glaucocalyxin A at various concentrations (typically 0-50 μM) for 24-72 hours. Cell viability is assessed using MTT or CCK-8 assays. Apoptosis is evaluated by flow cytometry using Annexin V-FITC/PI staining. Protein expression is analyzed by Western blot. For GPVI pathway studies, platelets are isolated and stimulated with collagen.
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| Animal Protocol |
In vivo studies for Glaucocalyxin A would be conducted in mouse xenograft models. Cancer cells (e.g., osteosarcoma, NSCLC, or breast cancer cells) would be implanted subcutaneously into immunodeficient mice. Once tumors reach a certain size, Glaucocalyxin A would be administered via oral gavage or intraperitoneal injection at appropriate doses. Tumor volumes would be measured twice weekly, and body weights monitored for toxicity. At study termination, tumors would be harvested for histology, immunohistochemistry, and Western blot analysis of PI3K/Akt pathway proteins and apoptosis markers.
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| ADME/Pharmacokinetics |
Specific pharmacokinetic data for Glaucocalyxin A are not extensively reported. As a diterpenoid with molecular weight 332.43 g/mol, the compound is expected to have moderate lipophilicity and potential for oral absorption. The compound is soluble in DMSO and formulated for in vivo administration. Formal PK studies would be required to determine parameters such as half-life, clearance, volume of distribution, and oral bioavailability. The compound's stability and protein binding properties would also need characterization.
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| Toxicity/Toxicokinetics |
Toxicological data for Glaucocalyxin A are limited but promising. The compound inhibits proliferation and promotes apoptosis in cancer cells in a dose-dependent manner but not in normal glial cells, suggesting some selectivity for cancer cells. As a natural product from Rabdosia rubescens, which has traditional medicinal uses, the compound is generally considered to have a moderate safety profile. However, comprehensive toxicology studies have not been reported. Glaucocalyxin A is also noted to have antiplatelet activity, which may affect bleeding risk.
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| References | |
| Additional Infomation |
According to reports, Glaucocalyxin A is found in Japanese chamomile, variegated chamomile, and other organisms with available data.
Glaucocalyxin A is an ent-kauranoid diterpenoid from Rabdosia rubescens with antitumor activity via PI3K/Akt pathway inhibition and mitochondrial apoptosis induction. It induces apoptosis in various cancer cell lines and shows anti-inflammatory and antiplatelet effects. No clinical trials or approvals exist. For research use only. |
| Molecular Formula |
C20H28O4
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|---|---|
| Molecular Weight |
332.4339
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| Exact Mass |
332.198
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| CAS # |
79498-31-0
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| Related CAS # |
79498-31-0
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| PubChem CID |
10471963
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| Appearance |
White to off-white solid
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
513.4±50.0 °C at 760 mmHg
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| Melting Point |
219.5-220.5℃
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| Flash Point |
278.4±26.6 °C
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| Vapour Pressure |
0.0±3.0 mmHg at 25°C
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| Index of Refraction |
1.574
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| LogP |
0.88
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
0
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| Heavy Atom Count |
24
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| Complexity |
650
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| Defined Atom Stereocenter Count |
7
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| SMILES |
OC1[C@@H]2C(C([C@@]31[C@H](O)C[C@@H]1C(C(CC[C@@]1(C)[C@@H]3CC2)=O)(C)C)=O)=C
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| InChi Key |
UCDVIBNDYLUWFP-MJTHGBBVSA-N
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| InChi Code |
InChI=1S/C20H28O4/c1-10-11-5-6-12-19(4)8-7-14(21)18(2,3)13(19)9-15(22)20(12,16(10)23)17(11)24/h11-13,15,17,22,24H,1,5-9H2,2-4H3/t11-,12-,13+,15+,17+,19-,20-/m0/s1
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| Chemical Name |
(1R,2R,4S,9R,10S,13S,16R)-2,16-dihydroxy-5,5,9-trimethyl-14-methylidenetetracyclo[11.2.1.01,10.04,9]hexadecane-6,15-dione
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| Synonyms |
Glaucocalyxin A
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: 50~66 mg/mL (150.4~198.5 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.52 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.52 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.52 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.0082 mL | 15.0408 mL | 30.0815 mL | |
| 5 mM | 0.6016 mL | 3.0082 mL | 6.0163 mL | |
| 10 mM | 0.3008 mL | 1.5041 mL | 3.0082 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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